Pyong Woo Park, PhD
|Hospital Title||Assistant in Medicine|
|Academic Title||Associate Professor of Pediatrics|
|Pyong Woo Park|
320 Longwood Avenue
Boston, MA 02115
The major goal of the Park Laboratory is to understand how components of the extracellular matrix (ECM) modulate the pathogenesis of infectious and non-infectious inflammatory diseases, with a particular focus on the role of proteoglycans and elastin in these processes. Historically known for its structural roles, the ECM is now known to regulate many cellular and physiological events. Dr. Park and his colleagues have found that several major bacterial pathogens (e.g., Pseudomonas aeruginosa, Staphylococcus aureus, Streptococcus pneumoniae) subvert the syndecan family of cell surface heparan sulfate proteoglycans to enhance their virulence in vivo. These bacterial pathogens stimulate syndecan shedding from the cell surface through specific virulence factors. Syndecan ectodomains bind to and inhibit several host defense factors, modulating the host environment to favor pathogenesis over eradication. These findings indicate that exploitation of syndecan shedding is an important pathogenic mechanism and suggest possible approaches to therapy.
The Park Laboratory has also found that syndecan shedding is activated in non-infectious inflammatory diseases. Here, syndecan ectodomains modulate inflammatory mediators and cells to attenuate inflammatory tissue injury. In sum, these data suggest that syndecan shedding is an important mechanism that assures the correct and adequate functioning of inflammation, but that certain pathogens have adapted or evolved to exploit this mechanism to promote their pathogenesis. On-going projects are focused on defining the molecular and cellular details of these mechanisms.
About Pyong Woo Park
Pyong Woo Park received a PhD from Washington University in St. Louis, Missouri, and completed a fellowship at Children's Hospital Boston and Harvard Medical School.
- Park, PW, Pier, GB, Hinkes, M and Bernfield, M, Exploitation of Syndecan-1 Shedding by Pseudomonas aeruginosa Enhances Virulence, Nature 2001; 411: 98-102.
- Li, Q, Park, PW, Wilson, CL, and Parks, WC, Matrilysin-mediated Shedding of Syndecan-1 Regulates Chemokine Mobilization and Transepithelial Efflux of Neutrophils in Acute Lung Injury, Cell, 2002; 111: 635-646.
- Bartlett, AH, Foster, TJ, Hayashida, A, and Park, PW, Alpha-toxin Facilitates the Generation of CXC Chemokine Gradients and Stimulates Neutrophil Homing in Staphylococcus aureus Pneumonia, J Infect Dis, 2008; 198: 1529-1535.
- Hayashida, K, Parks, WC, and Park, PW, Syndecan-1 Shedding Facilitates the Resolution of Neutrophilic Inflammation by Removing Sequestered CXC Chemokines, Blood, 2009; 114: 3033-3043.
- Hayashida, A, Amano, S, and Park, PW, Syndecan-1 Promotes Staphylococcus aureus Corneal Infection by Counteracting Neutrophil-mediated Host Defense, J. Biol. Chem., 2011; 286: 3288-3297.
- Teng, Y, Aquino, RS, and Park, PW, Molecular Functions of Syndecan-1 in Disease, Matrix Biol., 2012; 31: 3-16.